Open Access
ARTICLE
miR-181a-5p Promotes Proliferation and Invasion and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A)
* Department of Gynecology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, P.R. China
† Department of Anesthesia, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, P.R. China
Oncology Research 2018, 26(5), 703-712. https://doi.org/10.3727/096504017X14982569377511
Retracted 25 July 2024
A retraction of this article was approved in:
Retraction: miR-181a-5p Promotes Proliferation and Invasion and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A)
Read retraction
Abstract
Expression of miR-181a-5p associates with the proliferation and progression of cancer cells via its targets. This study was designed to investigate the effect of miR-181a-5p and its target inositol polyphosphate-5- phosphatase A (INPP5A) on the progression of cervical cancers. Upregulation of miR-181a-5p was revealed in the cervical cancer cell lines HeLa and SiHa in comparison with a normal cervical epithelium cell line End1/ E6E7 (p<0.001). The inhibition and upregulation of miR-181a-5p in cervical cancer cell lines significantly reduced or increased cell proliferation and invasion capacity, accompanied with enhanced or reduced apoptosis (p<0.05). Moreover, INPP5A overexpression significantly inhibited cell proliferation and invasion capacity and enhanced cell apoptosis. The target relationship of miR-181a-5p to INPP5A was demonstrated by both the results of the Dual-Luciferase Reporter Assay and the fact that the miR-181a-5p mimic attenuated INPP5A’s effect on cell proliferation, invasion, and apoptosis. To sum up, the overexpression of miR-181a-5p enhanced cell proliferation and invasion and inhibited apoptosis of cervical cancer cells by negatively targeting INPP5A. Therefore, inhibition of miR-181a-5p might benefit the inhibition of cervical cancer cell invasion.Keywords
Cite This Article
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.